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PTH Increases Ca++ Transport in Rat Brain Synaptosomes in Uremia

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New Actions of Parathyroid Hormone

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Abstract

Central nervous system (CNS) dysfunction is a major complication of patients with end stage renal failure. The clinical manifestations of this disorder are well described in several recent reviews (1). The biochemical basis for the CNS dysfunction of uremia is not well understood and is not completely corrected by dialysis. Studies of the CNS in humans and animals with renal failure have revealed no consistent pathologic changes (2) and biochemical studies in the brain of animal models of renal failure have also been generally unrevealing. The brain content of several ions (Na, K, Mg, Cl, bicarbonate) and water are normal (2,3), and so is brain intracellular pH (pHi) (3). Brain content of high-energy phosphate compounds (ATP, phosphocreatine) is also normal, although their turnover rate appears to be decreased (4). It appears that there may be altered permeability of the uremic brain to certain molecules, such as sodium, potassium, and inulin (5).

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Authors and Affiliations

  1. Divisions of Nephrology and Geriatrics, Department of Medicine Veterans Administration Medical Center and University of California, San Francisco, San Francisco, California, USA

    Cosmo L. Fraser & Allen I. Arieff

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  1. Cosmo L. Fraser
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  2. Allen I. Arieff
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Editors and Affiliations

  1. University of Southern California, Los Angeles, California, USA

    Shaul G. Massry

  2. Kobe University School of Medicine, Kobe, Japan

    Takuo Fujita

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© 1989 Plenum Press, New York

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Fraser, C.L., Arieff, A.I. (1989). PTH Increases Ca++ Transport in Rat Brain Synaptosomes in Uremia. In: Massry, S.G., Fujita, T. (eds) New Actions of Parathyroid Hormone. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0567-5_37

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  • DOI: https://doi.org/10.1007/978-1-4613-0567-5_37

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4612-7870-2

  • Online ISBN: 978-1-4613-0567-5

  • eBook Packages: Springer Book Archive

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